HomeLarge Type Edition
HOME ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Services
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
PubMed
Right arrow PubMed Citation

Journals of Gerontology Series A: Biological Sciences and Medical Sciences, Vol 54, Issue 10 B407-B417, Copyright © 1999 by The Gerontological Society of America


REVIEW, TUTORIAL

What counts in brain aging? Design-based stereological analysis of cell number

JM Long, PR Mouton, M Jucker and DK Ingram
Molecular Physiology and Genetics Section, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. LongJ@grc.nia.nih.gov

The advent and implementation of new design-based stereological techniques allows the quantification of cell number without the assumptions required when obtaining areal densities. These new techniques are rapidly becoming the standard for quantifying cell number, particularly in aging studies. Recently, studies using stereological techniques have failed to confirm earlier findings regarding age-associated neural loss. This newly emerging view of retained cell number during aging is having a major impact on biogerontology, prompting revaluation of long-standing hypotheses of age-related cell loss as causal for age-related impairments in brain functioning. Rather than focus on neuronal loss as the end-result of a negative cascade of neuronal injury, research has begun to consider that age-related behavioral declines may reflect neuronal dysfunction (e.g., synaptic or receptor loss, signal transduction deficits) instead of neuronal death. Here we discuss design-based stereology in the context of age-related change in brain cell number and its impact on consideration of structural change in brain aging. Emergence of this method of morphometrics, however, can have relevance to many areas of gerontological research.


This article has been cited by other articles:


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
E. Alberti, H. B. Mikkelsen, X. Y. Wang, M. Diaz, J. O. Larsen, J. D. Huizinga, and M. Jimenez
Pacemaker activity and inhibitory neurotransmission in the colon of Ws/Ws mutant rats
Am J Physiol Gastrointest Liver Physiol, June 1, 2007; 292(6): G1499 - G1510.
[Abstract] [Full Text] [PDF]


Home page
AM J ALZHEIMERS DIS OTHER DEMENHome page
R. J. Castellani, H.-g. Lee, G. Perry, and M. A. Smith
Antioxidant protection and neurodegenerative disease: The role of amyloid-{beta} and tau
American Journal of Alzheimer's Disease and Other Dementias, March 1, 2006; 21(2): 126 - 130.
[Abstract] [PDF]


Home page
J. Neurosci.Home page
D. E. Smith, P. R. Rapp, H. M. McKay, J. A. Roberts, and M. H. Tuszynski
Memory Impairment in Aged Primates Is Associated with Focal Death of Cortical Neurons and Atrophy of Subcortical Neurons
J. Neurosci., May 5, 2004; 24(18): 4373 - 4381.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
I. I. Kruman, T. S. Kumaravel, A. Lohani, W. A. Pedersen, R. G. Cutler, Y. Kruman, N. Haughey, J. Lee, M. Evans, and M. P. Mattson
Folic Acid Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons and Sensitize Them to Amyloid Toxicity in Experimental Models of Alzheimer's Disease
J. Neurosci., March 1, 2002; 22(5): 1752 - 1762.
[Abstract] [Full Text] [PDF]




HOME ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1999 by The Gerontological Society of America.